Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty.
Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty.
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DOI：
10.1038/s41569-018-0064-2
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发表时间：
2018-09
期刊：
影响因子：
--
通讯作者：
Fabbri E
中科院分区：
文献类型：
--
作者：
Ferrucci L;Fabbri E
大多数老年人会发生炎症，这是一种以血液炎症标志物水平升高为特征的疾病，其对慢性发病、残疾、虚弱和过早死亡具有高度易感性。炎症的潜在机制包括遗传易感性、向心性肥胖、肠道通透性增加、微生物群组成变化、细胞衰老、NLRP 3炎性小体激活、线粒体功能障碍引起的氧化应激、免疫细胞失调和慢性感染。炎症是心血管疾病（CVD）的危险因素，临床试验表明这种关联是因果关系。炎症也是慢性肾脏疾病、糖尿病、癌症、抑郁症、痴呆症和肌肉减少症的风险因素，但调节炎症是否有益于影响非CVD健康问题的临床过程是有争议的。这种不确定性是一个需要解决的重要问题，因为患有CVD的老年患者经常受到多发病和虚弱的影响-这会影响临床表现，预后和对治疗的反应-并且通过与CVD相似的机制与炎症相关。炎症通过抑制生长因子、增加促甲状腺激素和干扰稳态信号传导而影响CVD、多发性硬化和虚弱的假设得到了机制研究的支持，但需要在人类中得到证实。炎症的早期调节是否能预防或延迟心血管脆弱的发生，应该在临床试验中进行测试。
Most older individuals develop inflammageing, a condition characterized by elevated levels of blood inflammatory markers that carries high susceptibility to chronic morbidity, disability, frailty, and premature death. Potential mechanisms of inflammageing include genetic susceptibility, central obesity, increased gut permeability, changes to microbiota composition, cellular senescence, NLRP3 inflammasome activation, oxidative stress caused by dysfunctional mitochondria, immune cell dysregulation, and chronic infections. Inflammageing is a risk factor for cardiovascular diseases (CVDs), and clinical trials suggest that this association is causal. Inflammageing is also a risk factor for chronic kidney disease, diabetes mellitus, cancer, depression, dementia, and sarcopenia, but whether modulating inflammation beneficially affects the clinical course of non-CVD health problems is controversial. This uncertainty is an important issue to address because older patients with CVD are often affected by multimorbidity and frailty — which affect clinical manifestations, prognosis, and response to treatment — and are associated with inflammation by mechanisms similar to those in CVD. The hypothesis that inflammation affects CVD, multimorbidity, and frailty by inhibiting growth factors, increasing catabolism, and interfering with homeostatic signalling is supported by mechanistic studies but requires confirmation in humans. Whether early modulation of inflammageing prevents or delays the onset of cardiovascular frailty should be tested in clinical trials.
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